In severe head injury, CT scan and neurosurgical referral are important, and, if signs of brain herniation (Kellie-Monroe signs) are present or developing, simple but often effective means of decreasing the intracranial pressure should be ascertained and implemented:

1. The head should be elevated (30° to 45°). Keep the neck straight and avoid constriction of venous return.

2. Maintain normovolemia and normal blood pressure (BP) (mean BP > 90 mm Hg).

3. Ventilate to normocapnia and avoid hypocapnia (Pco2 >3.5 kPa).

4. Use light sedation and analgesia (e.g., codeine phosphate at 30 to 60 mg IM q4h).

5. Insert an ICP bolt to monitor the pressure status.

6. Consider administration of mannitol (1 g/kg IV immediately) (7).

Because of the likelihood of spinal injury, any patient with traumatic injury should be treated as having potential spinal injury until radiographic and clinical evidence indicates otherwise. Imaging of the spine should include at least plain x-ray films of the cervical spine (anteroposterior and lateral, a peg view, and with the C7-T1 junction visible). When a spinal injury is strongly suggested, either because of the mode of injury or because of indicative findings on the x-ray film, a CT scan of the spine should be performed next (8).

All physicians must remember that CT scanning is not an absolute diagnostic test. It is worth noting that spinal cord injury without noticeable radiographic abnormality occurs in up to 5% of spinal injuries (8).

Common types of injury that can be seen on CT include atlanto-occipital dislocation (usually fatal), atlas fractures (often treated conservatively), axis fractures (in most cases challenging), and C3-T1 injuries in which earliest alignment and decompression of the spinal cord is desirable (8).

Spinal cord trauma patients must be immediately assessed for proper localization and determination of the extent of the lesion. Physicians are reminded that in the acute phase, the classic syndrome of complete spinal cord transection presents with the following:

1. Possible respiratory insufficiency

2. Lower and upper extremity areflexia combined with anesthesia below the affected level

3. Neurogenic shock with hypothermia and hypotension without compensatory tachycardia (not observed commonly in low thoracic and lumbar spinal cord lesions)

4. Loss of rectal and bladder sphincter tone

5. Urinary and bowel retention leading to abdominal distention, ileus, and delayed gastric emptying (9)

Ipsilateral ptosis, miosis, and anhydrosis (Horner's syndrome) may also present because of interruption of the descending sympathetic pathways (9).

In the anterior cord syndrome, the patient presents with paralysis, loss of pain and temperature sensation below the level of the lesion, and relative sparing of touch, vibration, and proprioception.

Trauma commonly leads to central cord syndrome, often associated with significant arm weakness, less pronounced leg weakness, and variable sensory deficits. Pain and temperature sensations are affected most commonly, a modality known as "dissociated sensory loss" that may present in a cape-like fashion (8,9).

The other common traumatic presentations include Brown-Sequard syndrome (a hemicordectomy with ipsilateral paralysis, loss of vibration and position sense below the level of the lesion with hyperreflexia, while con-tralaterally, loss of pain and temperature sensation occurs two to three segments below the level of the lesion) and the cauda equina and conus medullaris syndromes (8-10).

Patients with lesions affecting only the cauda equina can present with a polyradiculopathy with pain, radicular sensory changes, asymmetric lower motor neuron-type leg weakness, and sphincter disturbances. This can be difficult to distinguish from involvement of the lumbosacral plexus or multiple nerves. Lesions affecting only the conus medullaris cause early disturbance of bowel/bladder function (11).

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